<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://www.biomedcentral.com/feeds/editorspicks?journal=bmcclinpathol&amp;quantity=">
        <title>Editor's picks</title>
        <link>http://www.biomedcentral.com/bmcclinpathol/</link>
        <description>The editor's pick of recent articles published by BMC Clinical Pathology</description>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1472-6890/12/7" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1472-6890/12/4" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1472-6890/11/14" />
                            </rdf:Seq>
        </items>
                 <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://www.biomedcentral.com/1472-6890/12/7">
        <title>Prognostic impact of CD57, CD68, M-CSF, CSF-1R, Ki67 and TGF-beta in soft tissue sarcomas</title>
        <description>Background:
Prognostic markers in curable STS may have the potential to guide therapy after surgical resection. The purpose of this study was to clarify the prognostic impact of the presence of cells and growth factors belonging to the innate immune system in soft tissue sarcomas (STS). The significance of macrophages (CD68), their growth factor macrophage colony-stimulating factor (M-CSF), its receptor colony-stimulating factor-1 receptor (CSF-1R), natural killer cells (CD57) and the general immunomodulating molecule (TGF-beta) are all controversial in STS. Herein, these markers are evaluated and compared to the cell proliferation marker Ki67.
Methods:
Tissue microarrays from 249 patients with non-gastrointestinal (non-GIST) STS were constructed from duplicate cores of viable and representative neoplastic tumor areas and duplicate cores of peritumoral capsule. Immunohistochemistry was used to evaluate the expression of CD68, M-CSF, CSF-1R, CD57, TGF-beta and Ki67 in tumor and peritumoral capsule.
Results:
In univariate analyses increased expression of M-CSF (P = 0.034), Ki67 (P &lt; 0.001) and TGF-beta (P = 0.003) in tumor correlated with shorter disease-specific survival (DSS). Increased expression of CD68 in tumor correlated significantly with malignancy grade (P = 0.016), but not DSS (P = 0.270). Increased expression of Ki67 in peritumoral capsule tended to correlate with a shorter DSS (P = 0.057). In multivariate analyses, co-expression of M-CSF and TGF-beta (P = 0.022) in tumor and high expression of Ki67 (P = 0.019) in peritumoral capsule were independent negative prognostic factors for DSS.
Conclusions:
Increased co-expression of M-CSF and TGF-beta in tumor in patients with STS, and increased expression of Ki67 in peritumoral capsule were independent negative prognostic factors for DSS.</description>
        <link>http://www.biomedcentral.com/1472-6890/12/7</link>
                <dc:creator>Sveinung W Sorbye</dc:creator>
                <dc:creator>Thomas K Kilvaer</dc:creator>
                <dc:creator>Andrej Valkov</dc:creator>
                <dc:creator>Tom Donnem</dc:creator>
                <dc:creator>Eivind Smeland</dc:creator>
                <dc:creator>Khalid Al-Shibli</dc:creator>
                <dc:creator>Roy M Bremnes</dc:creator>
                <dc:creator>Lill-Tove Busund</dc:creator>
                <dc:source>BMC Clinical Pathology 2012, 12:7</dc:source>
        <dc:date>2012-05-03T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1472-6890-12-7</dc:identifier>
                            <dc:title>Innate immunity markers in soft tissue sarcomas</dc:title>
                            <dc:description>Increased co-expression of M-CSF and TGF-beta in soft tissue sarcoma, and increased expression of Ki67 in peritumoral capsule are independent negative prognostic factors for survival, suggesting that innate immunity markers may serve as prognosticators in soft tissue sarcomas.</dc:description>
                <prism:require>/content/figures/1472-6890-12-7-toc.gif</prism:require>
                <prism:publicationName>BMC Clinical Pathology</prism:publicationName>
        <prism:issn>1472-6890</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2012-05-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1472-6890/12/4">
        <title>Relation of LAT1/4F2hc expression with pathological grade, proliferation and angiogenesis in human gliomas</title>
        <description>Background:
LAT1/4F2hc heterodimeric complex is a major route for the transport of large neutral essential amino acids through the plasma membrane. Although it has been shown that LAT1/4F2hc is highly expressed in a variety of human tumors including gliomas, and LAT1 over-expression is associated with glioma grade and poor prognosis of glioma patients, the precise tissue location of LAT1/4F2hc in gliomas and the precise role of LAT1/4F2hc in glioma biological features remain unclear.
Methods:
In the current study, the expressions of LAT1, 4F2hc, CD34 and Ki-67 were investigated by immunohistochemistry in 62 cases of human brain glioma; LAT1/4F2hc expression level, Ki-67 labeling index (Ki-67 LI) and microvessel density (MVD) were measured semi-quantitatively; and the correlation of LAT1/4F2hc expression with histopathological features, Ki-67 LI and MVD in gliomas was further analyzed.
Results:
The results showed that both LAT1 and 4F2hc were expressed in all examined specimens. LAT1 but 4F2hc expression levels significantly correlated with the pathological grade and both expression levels significantly correlated with Ki-67 LI of gliomas. We also demonstrated that both LAT1 and 4F2hc immunoreactivity were observed in tumor cells as well as vascular endothelia; furthermore, the LAT1 expression level was markedly associated with glioma MVD as well.
Conclusion:
LAT1/4F2hc over-expression is closely correlates with the malignant phenotype and proliferation of gliomas, and LAT1 was associates with glioma angiogenesis. LAT1/4F2hc, especially LAT1, may become a novel potential molecular target for glioma biological therapy.</description>
        <link>http://www.biomedcentral.com/1472-6890/12/4</link>
                <dc:creator>Zhen Haining</dc:creator>
                <dc:creator>Nobuyuki Kawai</dc:creator>
                <dc:creator>Keisuke Miyake</dc:creator>
                <dc:creator>Masaki Okada</dc:creator>
                <dc:creator>Shuichi Okubo</dc:creator>
                <dc:creator>Xiang Zhang</dc:creator>
                <dc:creator>Zhou Fei</dc:creator>
                <dc:creator>Takashi Tamiya</dc:creator>
                <dc:source>BMC Clinical Pathology 2012, 12:4</dc:source>
        <dc:date>2012-02-28T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1472-6890-12-4</dc:identifier>
                            <dc:title>Role of LAT1/4F2hc levels in glioma</dc:title>
                            <dc:description>Large-type amino acid transporter 1 (LAT1) and heavy chain of 4F2 cell surface antigen (4F2hc) are expressed in human gliomas and their expression levels correlate with pathological grade and proliferation, with LAT1 being associated with glioma angiogenesis.</dc:description>
                <prism:require>/content/figures/1472-6890-12-4-toc.gif</prism:require>
                <prism:publicationName>BMC Clinical Pathology</prism:publicationName>
        <prism:issn>1472-6890</prism:issn>
        <prism:volume>12</prism:volume>
        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2012-02-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1472-6890/11/14">
        <title>Molecular preservation by extraction and fixation, mPREF: a method for small molecule biomarker analysis and histology on exactly the same tissue</title>
        <description>Background:
Histopathology is the standard method for cancer diagnosis and grading to assess aggressiveness in clinical biopsies. Molecular biomarkers have also been described that are associated with cancer aggressiveness, however, the portion of tissue analyzed is often processed in a manner that is destructive to the tissue. We present here a new method for performing analysis of small molecule biomarkers and histology in exactly the same biopsy tissue.
Methods:
Prostate needle biopsies were taken from surgical prostatectomy specimens and first fixed, each in a separate vial, in 2.5 ml of 80% methanol:water. The biopsies were fixed for 24 hrs at room temperature and then removed and post-processed using a non-formalin-based fixative (UMFIX), embedded, and analyzed by hematoxylin and eosin (H&amp;E) and by immunohistochemical (IHC) staining. The retained alcohol pre-fixative was analyzed for small molecule biomarkers by mass spectrometry.
Results:
H&amp;E analysis was successful following the pre-fixation in 80% methanol. The presence or absence of tumor could be readily determined for all 96 biopsies analyzed. A subset of biopsy sections was analyzed by IHC, and cancerous and non-cancerous regions could be readily visualized by PIN4 staining. To demonstrate the suitability for analysis of small molecule biomarkers, 28 of the alcohol extracts were analyzed using a mass spectrometry-based metabolomics platform. All extracts tested yielded successful metabolite profiles. 260 named biochemical compounds were detected in the alcohol extracts. A comparison of the relative levels of compounds in cancer containing vs. non-cancer containing biopsies showed differences for 83 of the compounds. A comparison of the results with prior published reports showed good agreement between the current method and prior reported biomarker discovery methods that involve tissue destructive methods.
Conclusions:
The Molecular Preservation by Extraction and Fixation (mPREF) method allows for the analysis of small molecule biomarkers from exactly the same tissue that is processed for histopathology.</description>
        <link>http://www.biomedcentral.com/1472-6890/11/14</link>
                <dc:creator>Jeffrey R Shuster</dc:creator>
                <dc:creator>Raymond S Lance</dc:creator>
                <dc:creator>Dean A Troyer</dc:creator>
                <dc:source>BMC Clinical Pathology 2011, 11:14</dc:source>
        <dc:date>2011-12-21T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1472-6890-11-14</dc:identifier>
                            <dc:title>Dual diagnostic tests on single biopsies</dc:title>
                            <dc:description>A modified fixation process preserves prostatectomy tissue biopsy integrity, allowing histology and multiple
small molecule biomarker analyses to be performed on the same highly localised sample, enabling the
distinction between normal and cancer-containing tissue specimens.</dc:description>
                <prism:require>/content/figures/1472-6890-11-14-toc.gif</prism:require>
                <prism:publicationName>BMC Clinical Pathology</prism:publicationName>
        <prism:issn>1472-6890</prism:issn>
        <prism:volume>11</prism:volume>
        <prism:startingPage>14</prism:startingPage>
        <prism:publicationDate>2011-12-21T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>

